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Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

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Abnormal sensorimotor plasticity in migraine without aura patients.

Francesco Pierelli1, Elisa Iacovelli, Martina Bracaglia

  • 1IRCCS Neuromed, Pozzilli (IS), Italy "Sapienza" University of Rome, Department of Medicosurgical Sciences and Biotechnologies, Neurology Section, Rome, Italy "Sapienza" University of Rome, Department of Medicosurgical Sciences and Biotechnologies, Latina, Italy G.B. Bietti Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, Rome, Italy.

Pain
|May 23, 2013
PubMed
Summary

Migraine patients show abnormal long-term cortical plasticity between attacks. Paired associative stimulation (PAS) revealed altered motor-evoked potential (MEP) responses in migraine without aura (MO) patients, suggesting abnormal thalamic control.

Keywords:
High-frequency oscillationsPaired associative stimulationThalamocortical fibersTranscranial magnetic stimulation

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Area of Science:

  • Neuroscience
  • Clinical Neurology
  • Neurophysiology

Background:

  • Migraine is associated with abnormal cortical excitability and plasticity.
  • The interictal period in migraine patients exhibits paradoxical responses to sensory and transcranial magnetic stimulation (TMS).
  • Long-term cortical functional plasticity can be assessed using paired associative stimulation (PAS).

Purpose of the Study:

  • To investigate long-term cortical plasticity in migraine without aura (MO) patients during the interictal period.
  • To compare PAS-induced changes in motor-evoked potential (MEP) amplitudes between MO patients and healthy volunteers (HV).
  • To explore the relationship between cortical plasticity and thalamocortical activation in MO patients.

Main Methods:

  • Paired associative stimulation (PAS) was applied to 16 MO patients and 15 HV.
  • PAS involved 90 peripheral electrical ulnar nerve stimuli followed by TMS of the motor cortex with 10 ms (PAS10) or 25 ms (PAS25) delays.
  • Motor-evoked potential (MEP) amplitudes were recorded before and after PAS; somatosensory high-frequency oscillations (HFOs) were recorded in a subset of participants.

Main Results:

  • PAS10 significantly increased MEP amplitudes in MO patients (+35.9%) but decreased them in HV (-17.7%).
  • PAS25 significantly potentiated MEP amplitudes in HV (+55.1%) but showed only a slight, nonsignificant increase in MO (+18.8%).
  • A significant inverse correlation was found between PAS10-induced MEP changes and early HFO amplitudes (r=-0.81; P=.01), indicating reduced thalamocortical activation with impaired plasticity.

Conclusions:

  • Migraine without aura patients exhibit abnormal long-term cortical plasticity in the interictal period.
  • Altered thalamic control may underlie the observed abnormalities in cortical plasticity in migraine.
  • These findings suggest a potential role for thalamocortical dysfunction in the pathophysiology of migraine.